title: Treating chronic arsenic toxicity with high selenium lentil diets.
abstract: Arsenic (As) toxicity causes serious health problems in humans, especially in the Indo-Gangetic plains and mountainous areas of China. Selenium (Se), an essential micronutrient is a potential mitigator of As toxicity due to its antioxidant and antagonistic properties. Selenium is seriously deficient in soils world-wide but is present at high, yet non-toxic levels in the great plains of North America. We evaluate the potential of dietary Se in counteracting chronic As toxicity in rats through serum biochemistry, blood glutathione levels, immunotoxicity (antibody response), liver peroxidative stress, thyroid response and As levels in tissues and excreta. To achieve this, we compare diets based on high-Se Saskatchewan (SK) lentils versus low-Se lentils from United States. Rats drank control (0ppm As) or As (40ppm As) water while consuming SK lentils (0.3ppm Se) or northwestern USA lentils (<0.01ppm Se) diets for 14weeks. Rats on high Se diets had higher glutathione levels regardless of As exposure, recovered antibody responses in As-exposed group, higher fecal and urinary As excretion and lower renal As residues. Selenium deficiency caused greater hepatic peroxidative damage in the As exposed animals. Thyroid hormones, triiodothyronine (T3) and thyroxine (T4), were not different. After 14weeks of As exposure, health indicators in rats improved in response to the high Se lentil diets. Our results indicate that high Se lentils have a potential to mitigate As toxicity in laboratory mammals, which we hope will translate into benefits for As exposed humans.
authors.affiliation: Department of Ecosystem and Public Health, Faculty of Medicine, University of Calgary, Calgary, AB T2N 4Z6, Canada.
authors.forename: Shweta
authors.initials: S
authors.lastname: Sah
authors.forename: Albert
authors.initials: A
authors.lastname: Vandenberg
authors.forename: Judit
authors.initials: J
authors.lastname: Smits
mesh_terms: D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D000975:Antioxidants / Q000378:metabolism; D020261:Arsenic Poisoning / Q000178:diet therapy* / Q000188:drug therapy* / Q000652:urine; D001152:Arsenicals / Q000737:chemistry / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002908:Chronic Disease; D004032:Diet; D004797:Enzyme-Linked Immunosorbent Assay; D005243:Feces / Q000737:chemistry; D005978:Glutathione / Q000097:blood; D007074:Immunoglobulin G / Q000096:biosynthesis; D007668:Kidney / Q000737:chemistry / Q000378:metabolism; D027806:Lens Plant / Q000737:chemistry*; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011490:Protein Disulfide Reductase (Glutathione) / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012643:Selenium / Q000032:analysis; D018036:Selenium Compounds / Q000737:chemistry / Q000627:therapeutic use*; D013963:Thyroid Hormones / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001152:Arsenicals; D007074:Immunoglobulin G; D018036:Selenium Compounds; D013963:Thyroid Hormones; D011490:Protein Disulfide Reductase (Glutathione); D005978:Glutathione; D012643:Selenium
keywords: ALP; ALT; ANOVA; Ab; Arsenic toxicity; Arsenicosis; As; CK; Cl; ELISA; GGT; GLDH; GSH; Hg; High selenium lentil; ICP-MS; K; KLH; KSI; LSI; MDA; Na; Rat toxicity model; SDH; SK; SSI; Saskatchewan; Se; Selenium biofortification; T3; T4; TBARS; TP; [(GS)(2)AsSe](−); alanine transferase; alkaline phosphatase; analysis of variance; antibody; arsenic; chloride; creatinine kinase; enzyme linked immunosorbent assay; gamma glutamyl transferase; gamma lactate dehydrogenase; glutathione sulfhydryl; inductively coupled plasma-mass spectrometer; keyhole limpet hemocyanin; kidney somatic index; liver somatic index; malondialdehyde; mercury; potassium; selenium; seleno-bis-arsinium-ion; sodium; sorbitol dehydrogenase; spleen somatic index; thiobarbituric acid reactive substances; thyroxine; total protein; triiodothyronine